. Despite efforts by academics, prevention programs, and industry leaders, suicide rates have increased by 31% since 2001 and suicide remains the tenth leading cause of death in the United States. A major challenge is understanding what mechanisms confer proximal risk for lethal and near-lethal suicide attempts. Suicide attempts are most often preceded by an acute stressor and occur during brief periods characterized by extreme emotional distress. However, research to date has overwhelmingly collected data under neutral (e.g., unstressed, comfortable) laboratory conditions, limiting the field's ability to understand how potential mechanisms of risk operate during periods of acute stress. This is an unexplored area that can contribute to our knowledge of how promising mechanisms operate under stress and differ within and between individuals across time. Suicide attempts occur across many different disorders and can occur in the absence of a diagnosable disorder; therefore, a transdiagnostic approach to studying mechanisms associated with suicide risk is needed. Dysfunction in reward responsiveness and emotional reaction/regulation are two transdiagnostic factors that have helped distinguish suicide attempters from ideators during unstressed conditions. Neural activity related to reward responsiveness and emotional reaction/regulation capacity can be modulated by environmental stimuli and likely functions differently during periods of acute stress, but these claims have not yet been examined empirically. In addition, previous research on these factors has suffered from critical limitations such as cross-sectional research designs and a reliance on self-report data. The current study seeks to address these limitations by using a longitudinal design and multiple units of analysis (electroencephalography/event-related potentials [EEG/ERP], self-report) to examine how reward responsiveness and emotion regulation change under laboratory-induced stress (i.e., an attempt to elicit arousal mirroring aspects of a suicidal crisis).
Specific Aim 1 is to investigate the impact of stress on reward responsiveness and emotional reaction/regulation in individuals with a history of suicide attempt(s) compared to individuals with recent ideation.
Specific Aim 2 is to examine if neural activity related to reward responsiveness and emotional reaction/regulation capacity during acute stress is associated with current and/or future suicide risk. Exploratory aims will investigate intraindividual variability as well as how self-reported stress outside of the laboratory impacts reward responsiveness and emotion regulation over time. Investigating how reward responsiveness and emotional reactivity/regulation are impacted by arousal could offer important information on proximal risk and inform possible intervention targets during high risk periods. Further, this study directly addresses several objectives outlined in the Prioritized Research Agenda for Suicide Prevention (i.e., identify biomarkers and interactions associated with current/future risk, identify cognitive dysfunction associated with risk that may be amenable to intervention) and the first Strategic Objective outlined in the 2019 NIMH Strategic Plan, ?Define the mechanisms of complex behaviors.?
Suicide attempts most often occur after an acute stressor and during periods of high emotional distress; however, the overwhelming majority of suicide research has collected data under neutral (e.g., calm, unstressed) laboratory conditions, which severely limits our ability to understand how mechanisms related to suicide attempts may be impacted by acute stress. This study examines differences in how recent suicidal ideators and previous suicide attempters process rewards and regulate emotions during a laboratory-induced stressor using neurophysiological and self-report assessments with a longitudinal design. Findings may be analogous to how functioning in these areas is impacted during a suicidal crisis and inform future interventions, and will also examine if the investigated neural markers can track suicide risk over time.
